Mir-423-3p And EBV Case Study

An abnormality in this process leads to a number of problems, including cancer. MicroRNAs are a type of RNA which inhibit the expression of genes and play a vital role in the development of cancer. Of notable interest is miR-378, as it increases tumor angiogenesis and growth and also enhances the survival of these cells, by decreasing the expression of tumor suppression genes like Sufu. A study testing human cell lines found that when Sufu expression levels were high, miR-378 expression levels were low, and when Sufu levels were low, miR-378 levels were high, showcasing that the two were negatively correlated. Because repression of Sufu can lead to rampant proliferation of cells, the inhibition of Sufu is essential in order for miR-378 to promote angiogenesis and increase cell

miRNA shuttles offer stable gene silencing, flexibility in design, and effective delivery to target tissues with the help of AAV vectors, making their use an option worth exploring for treatment of various neuromuscular

Specific Aim #1. To determine the effect of miR200 family on human primary ATII cell biology and lung regeneration in IPF.

Hepatocellular carcinoma (HCC), a lethal liver cancer, has a very poor prognosis and is in dire need of novel targets to develop more effective treatments. The conventional treatment options of surgery and chemotherapy were limited to pre-metastatic HCC; however, a multi-kinase inhibitor, in addition to targeting other factors involved in development and progression of the disease showed promising results in advanced HCC [42]. LncRNAs such as HOTAIR, MALAT1, and H10 are dysregulated and have been suggested to play an essential role in HCC development whereas dysregulation affects proliferation, apoptosis, and metastasis. This is also true for gastric cancer, whereby dysregulation of lncRNAs- HOTAIR, HULC, and H19 are relatively linked to development, metastasis, and prognosis [43]. HCC is also characterized by aberrant expression of miRNAs. Respectively, upregulation and downregulation has been associated with invasion and metastasis, tumor progression, and drug resistance. Meng et al. proposed that aberrantly expressed miRNAs may regulate the expression of certain genes that control cell growth, migration, and invasion. In this study, the expression of miRNA in normal versus tumor tissue was investigated which led to the identification of overexpressed miR-21 in human HCC that could potentially serve as a target for regulating downstream events [44].

The miRNA:miRNA* duplex consists of a functional guide strand, which is preferentially loaded into the RNA-induced silencing complex (RISC), and a complementary passenger strand that is rapidly degraded . Each mature miRNA together with the RISC, which contains Argonaute 2 (AGO2) as the catalytic core, controls gene expression of its target mRNA through sequence specific interactions that result in either degradation or translational repression of the target mRNA{Filipowicz:2008fg}. The sequence specific interactions between a miRNA and its mRNA target depend on the first 2 to 8 nucleotides of a miRNA, the so called ‘miRNA seed’ sequence, which bind with varying complementarity to the 3’-untranslated region (UTR) or open reading frame (ORF) of a target mRNA{Bartel:2004vj}. Because miRNA target sequences are highly conserved, approximately 20 to 30% of all human genes are targets of miRNAs. In addition, a miRNA sequence can guide the regulation of several hundred different mRNAs allowing them to have numerous regulatory roles in both normal development and disease{He:2004jj,

are involved in regulating gene expression by methylation of the 4th Lysine residue on H3 histones. So far,

In addition to transcriptional regulation and epigenetic mechanisms, posttranscriptional regulation by microRNAs is also critically involved in the intracellular signaling of oligodendrocyte differentiation. Studies using transgenic mice in which microRNA processing is specifically disrupted in the oligodendrocyte lineage by way of Dicer enzyme knockout have shown that microRNA processing is indispensible for normal CNS myelination (Dugas et al., 2010), and that in vitro OPCs also fail to differentiate in the absence of mature microRNAs. Specifically, three microRNAs including miR-219, miR-138, and miR-338 are found to be elevated by 1-2 orders of magnitude during OPC differentiation into oligodendrocytes, and that miR-219 when induced alone, is sufficient to promote the differentiation (Dugas et al., 2010). The downstream target of miR-219, ELOVL7, is also identified as a main molecular component involved in the development of the Dicer mutant phenotype (Shin, Shin, McManus, Ptacek, & Fu, 2009), and that overexpression of ELOVL7 results in lipid accumulation, which is in turn suppressed by co-overexpression of miR-219. Other important target genes of the above mentioned microRNAs include PDGFRa, Sox6, and Hes5 (Dugas et al., 2010; X. Zhao et al., 2010), all of which serve to

This study aims to evaluate the prognostic effect of miRNA expression in stage II CRC patients. The research protocol follows the PRISMA-P (the Preferred Reporting

On the other hand, hyper activation of IRE1 can affect c-Jun NH2-termina kinase (JNK), Nfkβ and the process known as IRE1 dependent decay (RIDD), which has ability to decrease some mRNAs, microRNA (miRNAs), including (miR-17, miR-34a, miR-125b,and miR-96) (46) to reduce more loading of ER

Aim1.1 Testing miR-125a overexpression can be performed via transforming a retrovirus vector construct into E.coli plasmid to amplify the vector, following by isolation of plasmids using specific Mini-prep Kit. Then, plasmids are transfected into Human Embryonic Kidney 293 cell line (HEK293 cell) or CH12F3 cell line. To determine the efficiency of transfection, we monitored green fluorescent protein (GFP) reporter construct expression by conducting either immunofluorescent assay or fluorescence-activated cell sorting (FACS) 14. We transduce the virus containing miR-125a vector into primary B cells that is purified by mouse B cell isolation Kit and stimulated primarily with LPS followed by second stimulation using LPS and IL-4. Cells were collected 60 h later for qRT-PCR and RNA extraction, or 96 h later for surface Ig analysis by FACS. The stimulated B cells are stained with CD19 and CD138 to measure the percentages of switched B cells by FACS. We predict a reduction in IgG1, IgG3, and CD138 populations due to the impede function in CSR and plasma cell differentiation due to miR-125a expression, which target Aicda and Prdm1. In addition, RNA extraction will be

Saumet et al. in 2008 observed that miR-23a~27a~24-2 is directly repressed by the PML-RARA oncogene. also in some study upregulation of miR-23a has been observed in cancers(22). Considerable up-regulation of miR-23a was reported by Meng and Gottardo in human bladder cancer and in malignant cholangiocytes compared to normal tissues. Furthermore, Mi et al. in their study showed that miR-23a was among several other miRNAs that have been differentially expressed between acute myeloid leukemia (AMLs) and acute lymphoblastic leukemia (ALLs). In addition, up-regulation of miR-23a/b along with miR-24 has also been identified in osteoblast cell line (20,21).

A very promising approach for understanding the involvement of a certain miRNA in the process of a disease such as cancer, is to assess the miRNA expression profile of cancer patients, and to compare with their normal counterpart is a very promising approach for understanding the involvement of a certain miRNA in a disease of interest. This may lead to the discovery of a novel prognostic or diagnostic biomarker. Although, it is believed that miRNA profile from extracted total cellular RNA is an actual indicator of RISC complex-associated miRNA, due to quick degradation of non-guide miRNA, this hypothesis was challenged by the Cullen group, when they compared the miRNA profile of the total cellular miRNAs with the

However, the mechanism regulating the migration of mature ecRNAs into the cytoplasm remains unclear. The linear counterparts of circRNAs, such as mRNAs or lncRNAs, can penetrate the nuclear membrane through the nuclear pore complex. Therefore, some researchers put forward the hypothesis that ecRNA export may be regulated by a mechanism similar to the regulatory mechanism of linear RNA migration [18]. The degradation pathway of circRNAs is another unanswered question. The expression level of circRNA is dynamically modulated by the balance between biogenesis and degradation of circRNAs. CircRNAs may be degraded by short interfering RNAs [13]. A recent study found that circRNAs may be cleared by extracellular vesicles or microvesicle release in mammalian cells [43]. However, this conclusion is based on an in vitro study. Whether circRNAs are degraded in vivo by a similar mechanism still needs further

Just after the Valadi’s discovery in 2007(59), various studies have been performed, in order to characterize exosomal miRNA as diagnostic biomarkers for cancers. In 2008, Taylor et al. reported that eight miRNAs, including miR-21, miR-141, miR-200a, miR-200c, miR-200b, miR-203, miR-205 and miR-214, previously demonstrated as diagnostic markers for ovarian cancer, were also present in serum exosomes, isolated from the ovarian cancer patients (74). In 2009, Rabinowits and collegues carried out a miRNA-profiling analysis on tumor biopsy specimen, exosomes isolated from lung adenocarcinoma patients and control subjects. They found a similar miRNA profile between exosomes and tumor biopsy samples from

It has been found that miRNAs in circulating exosomes are representative of those upregulated in the primary tumor cells16. In a separate study, Ohuchida et al. distinguished 24 miRNAs with altered expression in gemcitabine-resistant cells, and furthermore found that patients with high miR-142-5p and miR-204 expression had significantly longer survival times than those with low miR-142-5p and miR-204 expression in the